Plasma Catecholamine Metabolite Levels in ADHD Boys With and Without Reading Disabilities

Halperin, Jeffrey M.; Newcorn, Jeffrey H.; Schwatrz, Susan T.; McKay, Kathleen E.; Bedi, Gail; Sharma, Vanshdeep

doi:10.1207/s15374424jccp2202_8

Cited by 14 publications

(7 citation statements)

References 30 publications

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“…Since the studies of Halperin et al [22,23] emphasized reading problems, we examined a below average grade‐school performance in mathematics, reading, and writing separately. This was done by a χ 2 analysis of the NE gene score versus scoring the mathematics, reading, and writing performance as ‘average’ or ‘above average’=0, and ‘below average’=1.…”

Section: Resultsmentioning

confidence: 99%

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Additive effect of three noradrenergic genes (ADRA2A, ADRA2C, DBH) on attention‐deficit hyperactivity disorder and learning disabilities in Tourette syndrome subjects

et al. 1999

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Halperin et al. (Halperin JM. Newcorn JH, Koda VH, Pick L, McKay KE, Knott P. Noradrenergic mechanisms in ADHD children with and without reading disabilities: a replication and extension. J Am Acad Child Adolesc Psychiatry 1997: 36: 1688 1696) reported a significant increase in plasma norepinephrine (NE) in attention-deficit hyperactivity disorder (ADHD) children with reading and other cognitive disabilities compared to ADHD children without learning disabilities (LD). We examined the hypothesis that ADHD + LD was associated with NE dysfunction at a molecular genetic level by testing for associations and additive effects between polymorphisms at three noradrenergic genes the adrenergic alpha2A receptor (ADRA2A), adrenergic alpha2C receptor (ADRA2C), and dopamine beta-hydroxylase (DBH) genes. A total of 336 subjects consisting of 274 individuals with Tourette syndrome (TS) and 62 normal controls were genotyped. Regression analysis showed a significant correlation between scores for ADHD, a history of LD, and poor grade-school academic performance that was greatest for the additive effect of all three genes. Combined, these three genes accounted for 3.5% of the variance of the ADHD score (p = 0.0005). There was a significant increase in the number of variant NE genes progressing from subjects without ADHD (A-) or learning disorders (LD-) to A + LD - to A - LD + to A + LD + (p = 0.0017), but no comparable effect for dopamine genes. These data support an association between NE genes and ADHD, especially in ADHD + LD subjects.

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Section: Resultsmentioning

confidence: 99%

“…In 1993, Halperin et al [22] reported that boys with ADHD and reading disabilities had significantly higher plasma MHPG levels than boys with ADHD only. They replicated this finding in 1997 [23] in a study of an additional 25 children.…”

Section: Attention‐deficit Hyperactivity Disorder (Adhd) With and Witmentioning

confidence: 99%

Additive effect of three noradrenergic genes (ADRA2A, ADRA2C, DBH) on attention‐deficit hyperactivity disorder and learning disabilities in Tourette syndrome subjects

et al. 1999

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“…147,148 Destruction of the ascending dorsal NE bundle results in an animal that is unable to filter out irrelevant stimuli. 149 The studies of Halperin et al 150,151 found that plasma MHPG levels were significantly higher in ADHD children with reading disabilities than in children without reading disabilities. They also showed a significant negative correlation between the plasma levels of MHPG and measure of verbal IQ.…”

Section: A Norepinephrine (Ne) Modelmentioning

confidence: 99%

Clinical and Molecular Genetics of ADHD and Tourette Syndrome

Comings

2001

Annals of the New York Academy of Sciences

134

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ADHD is a polygenic disorder due to the additive effect of genes affecting dopamine, norepinephrine, serotonin, GABA, and other neurotransmitters. Some of the specific loci involved are dopamine genes—DRD2, DRD4, DRD5, and the dopamine transporter; norepinephrine (NE) and epinephrine (EPI) genes—dopamine b‐hydroxylase, ADRA2A, ADRA2C, PNMT, norepinephrine transporter, MAOA, COMT; serotonin genes—TDO2, HTR1A, HTR1DA, serotonin transporter; GABA genes—GABRB3; androgen receptor and other genes. This model is consistent with all of the present knowledge about ADHD including (a) the increased frequency of ADHD in the relatives of ADHD probands, (b) the presence of a wide spectrum of comorbid behaviors (depression, anxiety, learning, conduct, oppositional‐defiant, conduct and substance abuse disorders) in ADHD probands and their relatives on both parental sides, (c) the close relationship to Tourette syndrome (TS), (d) the failure to find the genes for TS using linkage analysis, (e) the brain imaging studies showing hypometabolism of the frontal lobes, (f) the relationship between dopamine D2 receptor density and regional blood flow, (g) the correlation between tics and dopamine D2 receptor density in TS, (h) the motor hyperactivity of dopamine transporter and dopamine D3 receptor gene knockout mice, (i) the LeMoal and Shaywitz dopamine deficiency animal models of ADHD, (j) the NE models of ADHD, (k) the failure to explain ADHD on the basis of any single neurotransmitter defect, (l) the response of ADHD to dopamine and a2‐adrenergic agonists, (m) the small percentage of the variance of specific behaviors accounted for by each gene, and numerous other aspects of ADHD. The implications of the polygenic model for the understanding, diagnosis and treatment of ADHD and TS, as well as other psychiatric disorders, are reviewed.

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“…Some researchers have tried to quantify ADHD behaviors by systematic observation of "off task behavior" or by using mechanical devices to measure leg movements or restlessness. Measurement of catecholamines or metabolites in plasma and urine has been implemented with mixed success [Halperin et al, 1993;Pliszka et al, 1994]. The current consensus (as stated in DSM-IV) is that no laboratory tests reliably predict ADHD.…”

Section: Epidemiologic Case Definitionmentioning

confidence: 99%

The epidemiology of attention‐deficit/hyperactivity disorder (ADHD): A public health view

Rowland

Lesesne

Abramowitz

2002

Ment. Retard. Dev. Disabil. Res. Rev.

392

275

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Attention-deficit/hyperactivity disorder (ADHD) is the most common neurodevelopmental disorder of childhood. However, basic information about how the prevalence of ADHD varies by race/ethnicity, sex, age, and socio-economic status remains poorly described. One reason is that difficulties in the diagnosis of ADHD have translated into difficulties developing an adequate case definition for epidemiologic studies. Diagnosis depends heavily on parent and teacher reports; no laboratory tests reliably predict ADHD. Prevalence estimates of ADHD are sensitive to who is asked what, and how information is combined. Consequently, recent systematic reviews report ADHD prevalence estimates as wide as 2%-18%. The diagnosis of ADHD is complicated by the frequent occurrence of comorbid conditions such as learning disability, conduct disorder, and anxiety disorder. Symptoms of these conditions may also mimic ADHD. Nevertheless, we suggest that developing an adequate epidemiologic case definition based on current diagnostic criteria is possible and is a prerequisite for further developing the epidemiology of ADHD. The etiology of ADHD is not known but recent studies suggest both a strong genetic link as well as environmental factors such as history of preterm delivery and perhaps, maternal smoking during pregnancy. Children and teenagers with ADHD use health and mental health services more often than their peers and engage in more health threatening behaviors such as smoking, and alcohol and substance abuse. Better methods are needed for monitoring the prevalence and understanding the public health implications of ADHD. Stimulant medication is the treatment of choice for treating ADHD but psychosocial interventions may also be warranted if comordid disorders are present. The treatment of ADHD is controversial because of the high prevalence of medication treatment. Epidemiologic studies could clarify whether the patterns of ADHD diagnosis and treatment in community settings is appropriate. Population-based epidemiologic studies may shed important new light on how we understand ADHD, its natural history, its treatment and its consequences.

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Plasma Catecholamine Metabolite Levels in ADHD Boys With and Without Reading Disabilities

Cited by 14 publications

References 30 publications

Additive effect of three noradrenergic genes (ADRA2A, ADRA2C, DBH) on attention‐deficit hyperactivity disorder and learning disabilities in Tourette syndrome subjects

Additive effect of three noradrenergic genes (ADRA2A, ADRA2C, DBH) on attention‐deficit hyperactivity disorder and learning disabilities in Tourette syndrome subjects

Clinical and Molecular Genetics of ADHD and Tourette Syndrome

The epidemiology of attention‐deficit/hyperactivity disorder (ADHD): A public health view

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